ArticleJournal of molecular histology2026
The expression and mechanism of action of ADAMTS18 in endometrial cancer.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aimed to measure ADAMTS18 expression in endometrial carcinoma (EC), atypical hyperplasia (AH), and normal endometrium, and determine its biological role in EC. Retrospectively, we analyzed clinicopathological data of the following groups: EC group (n = 64, endometrioid adenocarcinoma), AH group (n = 55), and control group (CON, n = 64, normal). ADAMTS18 expression was detected via immunohistochemical staining/immunofluorescence assay. Ishikawa EC cells were used in the following groups: ADAMTS18 group (overexpression plasmid), CON group (untreated), and NC group (null plasmid). The effects of ADAMTS18 on cell proliferation (CCK-8), migration/invasion (Transwell), and apoptosis (TUNEL) were assessed. ADAMTS18 expression was the lowest in the EC group and the highest in the CON group (P < 0.05). In Ishikawa cells, compared to the NC/CON groups, ADAMTS18 overexpression significantly decreased cell proliferation (after 72 h and 96 h), migration, and invasion, and enhanced cell apoptosis (all P < 0.05). Low ADAMTS18 expression was correlated with higher FIGO stage (≥ III) and larger tumor diameter (≥ 2 cm) in EC. ADAMTS18 downregulation was correlated with the poor prognosis of EC and suppressed tumor proliferation/invasion in vitro. ADAMTS18 overexpression modulated the behavior of EC cells by inhibiting their proliferation, invasion, and migration, and promoting their apoptosis. Functioning as a tumor suppressor, ADAMTS18 is a potential therapeutic target in EC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.